98-230 EP The overall goal of this project is to elucidate the mechanism of one of the major complications of diabetes. Diabetic retinopathy and peripheral neuropathy are the leading causes of blindness and peripheral nerve damages respectively but the factors which initiate cell damage and lead to diabetic retinopathy and peripheral neuropathy are not known. Although current dogma implicates hyperglycemia, the null hypothesis has not been tested. It is impossible to dissociate the relative roles of insulin deficiency and hyperglycemia on complications with patients with established diabetes. However, reports of classical appearing diabetic retinopathy and other microvascuklar complications in patients without hyperglycemia suggest that these complications may not depend solely on hyperglycemia. Therefore, we hypothesize that insulin resistance, per se, contributes to early complications. Our specific aim is to determine if patients with insulin resistance but without hyperglycemia as part of the polycystic ovary syndrome (PCOS) exhibit retinal and/or peripheral nerve dysfunction which precedes symptomatics complications. We will conduct a masked, cross-sectional study of retinal and peripheral nerve function in women with PCOS who have been previously studied and who are known to have insulin resistance; some of the PCOS patients have impaired glucose tolerance but do not have diabetes. These patients will have normal retinal and neuromuscular examinations by standard criteria. We predict that 20-30% of the insulin resistant PCOS patients will have retinal dysfunction as reflected by impaired color vision or contrast sensitivity or decreased oscillatory potential amplitudes in their electroretinograms, or abnormal peripheral nerve conduction studies versus none of the normal controls. We hope to detect the earliest lesions which would in time lead to clinical symptoms of visual loss and impaired hand and foot sensation. In this way, the mechanism of retinopathy and neuropathy could be better determined and improved prophylactic therapies designed.